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Chapter: Basic & Clinical Pharmacology : Agents Used in Cardiac Arrhythmias

Adenosine - Antiarrhythmic Agents

Adenosine is a nucleoside that occurs naturally throughout the body. Its half-life in the blood is less than 10 seconds.

ADENOSINE

Mechanism & Clinical Use

Adenosine is a nucleoside that occurs naturally throughout the body. Its half-life in the blood is less than 10 seconds. Its mecha-nism of action involves activation of an inward rectifier K+ current and inhibition of calcium current. The results of these actions are marked hyperpolarization and suppression of calcium-dependent action potentials. When given as a bolus dose, adenosine directly inhibits AV nodal conduction and increases the AV nodal refrac-tory period but has lesser effects on the SA node. Adenosine is currently the drug of choice for prompt conversion of paroxysmal supraventricular tachycardia to sinus rhythm because of its high efficacy (90–95%) and very short duration of action. It is usually given in a bolus dose of 6 mg followed, if necessary, by a dose of 12 mg. An uncommon variant of ventricular tachycardia is adenosine-sensitive. The drug is less effective in the presence of adenosine receptor blockers such as theophylline or caffeine, and its effects are potentiated by adenosine uptake inhibitors such as dipyridamole.

Toxicity

Adenosine causes flushing in about 20% of patients and shortness of breath or chest burning (perhaps related to bronchospasm) in over 10%. Induction of high-grade AV block may occur but is very short-lived. Atrial fibrillation may occur. Less common tox-icities include headache, hypotension, nausea, and paresthesias.

The Nonpharmacologic Therapy of Cardiac Arrhythmias

It was recognized over 100 years ago that reentry in simple in vitro models (eg, rings of conducting tissues) was permanently interrupted by transecting the reentry circuit. This concept is now applied in cardiac arrhythmias with defined anatomic pathways—eg, atrio-ventricular reentry using accessory pathways, atrioventricular node reentry, atrial flutter, and some forms of ventricular tachy-cardia—by treatment with radiofrequency catheter ablation or extreme cold, cryoablation. Mapping of reentrant pathways and ablation can be carried out by means of catheters threaded into the heart from peripheral arteries and veins. Recent studies have shown that paroxysmal and persistent atrial fibrillation may arise from one of the pulmonary veins. Both forms of atrial fibrilla-tion can be cured by electrically isolating the pulmonary veins by radiofrequency catheter ablation or during concomitant cardiac surgery.

Another form of nonpharmacologic therapy is the implantablecardioverter-defibrillator (ICD), a device that can automaticallydetect and treat potentially fatal arrhythmias such as ventricular fibril-lation. ICDs are now widely used in patients who have been resusci-tated from such arrhythmias, and several trials have shown that ICD treatment reduces mortality in patients with coronary artery disease who have an ejection fraction  30% and in patients with class II or III heart failure and no prior history of arrhythmias. The increasing use of nonpharmacologic antiarrhythmic therapies reflects both advances in the relevant technologies and an increasing appreciation of the dangers of long-term therapy with currently available drugs.


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Basic & Clinical Pharmacology : Agents Used in Cardiac Arrhythmias : Adenosine - Antiarrhythmic Agents |


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